This invention relates to a system for the enhancement of the neurophysiological processes of a person, in particular those processes associated with reading, writing and speech. The invention was conceived in the context of treating reading, writing and speech disorders but has far broader applications including the treatment of Attention Deficit Hyperactivity Disorder (ADHD) and the enhancement of a person's perception of movement required for example, by sportspeople or defence force personnel.
Since the late nineteenth century it has become increasingly noticeable that a substantial percentage of the population possess no abnormalities in conventional vision, hearing or intelligence, yet display debilitating disorders of reading, writing and speech.
Although there is a connection between these different types of disorders, reading disorders have attracted the most concern and attention and are thought to afflict up to 15% of the world's population. Reading disorders are psychologically and economically damaging to a person, are largely hereditary and have been considered to be incurable.
A growing body of neuroscientific research has linked many of such disorders with neural debilitation's in different areas of the brain.
Several groups of scientists utilising modern non-invasive diagnostic techniques such as functional Magnetic Resonance Imaging (fMRI) or Positron Emission Tomography (PET) have found significant differences in brain activity, in particular in areas of the brain associated with the perception of movement, between those with reading disorders and those without.
The perception of sight begins when visible light contacts the retina at the back of the eye. Photoreceptor cells known as rods and cones are stimulated by this light to produce electrical impulses. These impulses travel from the retinal ganglion cells via their axons and ultimately connect with the visual centres of the brain, in particular the visual cortex. The connection between the retina and the visual cortex includes a small midbrain nodule called the lateral geniculate body. This body is divided into two layers, one of which is part of the magnocellular pathway and the other a part of the parvocellular pathway. The divided signal from these visual pathways continues to the visual cortex and the extrastriate visual cortex at the back of the brain to undergo a multiplicity of complex processes to emerge as a perception of sight.
The magnocellular and parvocelluar systems are part of the retino-geniculo-cortical pathway system. The magnocellular pathway has evolved to be able to process rapid movements of low contrast images in conditions of low luminance but with relatively poor colour sensitivity, whereas the parvocellular pathway processes fine stationary detail in conditions of brightness and with greater colour sensitivity.
Research has shown that both pathways are parallel processing systems involved in developing and sustaining an acute kind of depth perception called stereopsis. The magnocellular system is responsible for motion stereopsis, which is vital for normal reading. The parvocellular system is responsible for static stereopsis. Deficiencies in either pathway can affect stereopsis which can lead to an inability of a person to property process visual images.
Furthermore, it has been suggested in some research that the debilitation of receptive cell fields in the magnocellular pathway causes this parallel processing system to deliver mistimed visual information to the visual cortex. This, it has been hypothesised, causes instability of viewed text in some patients resulting in their reading disabilities.
The visual system is predominantly edge seeking and motion biased in character. Holding a steady fixation on a visual target is indeed not possible. When a steady fixation is induced in a laboratory, the visual image fades.
Oculographic recordings have demonstrated three types of eye movements that occur during fixation: microsaccades, (small, high-speed adjustments of fixation), fixation drift and high frequency tremors.
Saccades used in normal vision bring items of visual interest into the foveal area of the retina for examination under conditions of maximum acuity. Microsaccades are similar to saccades, except that the amplitudes are smaller.
Microsaccades occur about 2 to 3 times per second, along with a slow fixation drift, which in combination prevent fading of the retinal image. The manner in which microsaccades and fixation drifts are interposed is dependent upon an individual's optokinetic control. Such control is in turn influenced by neurophysiological debilitations that are partially non-visual in source.
Oculographic recordings have shown that during reading a stereotyped “staircase” pattern of eye movements occurs, consisting of alternating saccades and periods of fixation. During the pauses, semantic identification and recognition of characters is thought to occur. Each saccade moves the fovea (the portion of vision with the greatest acuity), about eight characters to the right. At the end of a line, a large saccade to the beginning of the next line occurs and the behaviour is repeated.
An optokinetic deficit could lead to reading disorders if it prevents microsaccades from occurring at the required speed and endurance, and if it prevents fixation drift to be controlled with enough endurance. If this deficit is compounded by some language or phonological impairment, then semantic recognition, an essential link in the reading chain, can be even more difficult to achieve.
During more rapid normal reading or the normal viewing of more complex visual images, the eyes employ a healthy motion and static stereopsis (depth perception) to find visual ‘cues’. They pause at very small time intervals and look directly at what the brain considers are the more important visual elements and deduces what is in between.
It has been suggested that some normal readers employ a strategy that uses “habitually preferred” patterns stored in their memory. This involves an initial visual scanning phase described as to “look without seeing” in which an internal model is formed in order to then “see without looking”. Finally, there is a rapid model verification phase to “look and see”. This requires rapid saccades to move the high acuity area of the fovea to the salient features for verification.
An ability to provide the required saccades, control of fixation drift, recognition of semantics, stereopsis and an adequate visual working memory, are essential prerequisites for good reading.
Furthermore, because of the relationship within the brain of the magnocellular and parvocellular pathways with other neurophysiological processes such as speech, hearing and kinaesthetic and somatosensory processes, an inability to properly process visual images can lead to disorders in these other processes.
From the large numbers of reading disorder treatment providers, few have attempted to search for curative solutions, particularly based on visual causes, in the belief that cures are not possible. Indeed most reading disorder associations and much of the scientific community still support this view.
The beginnings of a visual based curative approach commenced with the development of a simple apparatus called the CAM visual stimulator, developed in Cambridge England in the mid 1970s. The CAM stimulator was developed not for the treatment of reading disorders, but for the orthoptic treatment of pathologic binocularity, a condition where fixation errors of the eyes cause the brain to favour signals from a dominant eye and tends to suppress signals from the weaker eye. The stimulator comprised rotating paper discs covered with painted gratings intended for visual stimulation. This apparatus gained wide interest and exposure for the orthoptic treatment of ocular fixation disorders but with limited success.
Another version of the CAM apparatus was developed in Australia in the late 1970s, and comprised similar rotating discs with painted gratings, but with the addition of a diffuse light source from between the gratings. This second version of the CAM apparatus was the subject of Australian patent application no. 70697/81 by A. M. Lawson. It was also conceived and originally used for the same treatment of pathologic binocularity, although later was used for treatment of visual dyslexia.
Whilst these prior art apparatus achieved some success in treating the fixation disorders for which they were designed, their success in treating reading disorders was limited due to the complex nature of the retino-genicular-cortical pathways and the very limited range of stimulations that the rotating discs could provide. The edges of the stripes that provided the visual cues to the patient had a constant locus of movement, that being a circular path, and only provided the correct stimulation to a limited number of cells in the visual cortex and for a brief period of time as the edge passed through a particular orientation. The only variation in the stimulation was achieved by changing the disc to one with a different spacing and width of stripes. This variation could not be achieved without disruption to the patient's treatment.
The present invention seeks to provide apparatus and method wherein a patient can receive a more complete set of stimulations than was possible with the prior art.